FliA regulates the antibacterial activity of plantaricin BM-1 against Escherichia coli K-12 through the LuxS/AI-2 quorum-sensing-mediated biofilm formation

The inhibition rate (I%) of plantaricin BM-1 (3.75 mg/mL) against <i>E. coli</i> JW1907 (89.22 ± 1.13%) at the 8th h of culture was significantly higher than that of <i>E. coli</i> BW25113 (70.36 ± 6.30%) and ReJW1907 (74.75 ± 4.99%). The biofilm biomass produced by <i>E. coli</i> BW25113 (OD₅₉₅ _<i>nm</i> = 0.343 ± 0.056) was significantly reduced to 0.227 ± 0.04 after <i>fliA</i> deletion, and was recovered to its original level (0.358 ± 0.027) after <i>fliA</i> complement. A total of 205 DEGs were identified between <i>E. coli</i> BW25113 and JW1907. Among these, four DEGs (<i>fliZ</i>,<i>wza</i>, <i>lsrR</i>, and <i>pgaA</i>) were enriched in the biofilm formation pathway. Further analysis revealed eight up-regulated DEGs (<i>lsrKRBDCAFG</i>), which were significantly enriched in the LuxS/AI-2 quorum sensing (QS) system. After the deletion of any gene from <i>lsrKRBDCAFG</i>, the I% of plantaricin BM-1 against <i>E. coli</i> BW25113 (70.77 ± 7.01%) was significantly increased to 80.68-90.06%, with its biofilm production (0.254 ± 0.014) reduced to 0.135-0.188. In conclusion, FliA modulates biofilm formation through the LuxS/AI-2 QS system, thereby regulating the antibacterial activity of plantaricin BM-1. Overall, these findings improve our understanding of the bacteriostatic mechanism of class IIa bacteriocins against gram-negative bacteria.